Dihydrotestosterone and the Concept of 5α–Reductase Inhibition in Human Benign Prostatic Hyperplasia

  title={Dihydrotestosterone and the Concept of 5$\alpha$–Reductase Inhibition in Human Benign Prostatic Hyperplasia},
  author={Georg Bartsch and Roger S. Rittmaster and Helmut Klocker},
  journal={European Urology},
  pages={367 - 380}
Objective:The development of the human benign prostatic hyperplasia clearly requires a combination of testicular androgens and aging. Although the role of androgens as the causative factor for human benign prostatic hyperplasia is debated, they undoubtedly have at least a permissive role. The principal prostatic androgen is dihydrotestosterone (DHT). Although not elevated in human benign prostatic hyperplasia, DHT levels in the prostate remain at a normal level with aging, despite a decrease in… 
The Role of 5α-Reductase in Prostate Disease and Male Pattern Baldness
This review focuses first on the significance of enzyme-mediated conversion of T to DHT in the prostate and then on the medical applications of enzyme inhibitors for treatment of prostatic diseases and skin disorders where androgen metabolism may be up-regulated by 5α-reductase.
Androgens in Prostate Cancer and Benign Prostatic Hyperplasia
In aging men the prostate is of clinical significance as the site for two common diseases, benign prostatic hyperplasia (BPH) and prostate carcinoma (PCa), and the frequency of clinical diagnosis and interest in these diseases has increased.
Hormonal treatment of patients with benign prostatic hyperplasia: Pros and cons
It is indicated that finasteride has a role in the management of larger prostates and is a less morbid problem for the elderly than the potential syncope associated with the use of alpha blockers.
Serotonin regulates prostate growth through androgen receptor modulation
Evidence is presented that links 5-HT depletion to BPH etiology through modulation of AR and that Serotoninergic prostate pathway should be explored as a new therapeutic target for BPH.
Pao Pereira Extract Attenuates Testosterone-Induced Benign Prostatic Hyperplasia in Rats by inhibiting 5α-Reductase
It is suggested that Pao extract may be a promising and relative safe agent for BPH because it suppresses testosterone-induced BPH development through inhibiting AR activity and expression.
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Benign Prostatic Hyperplasia: Pathogenesis and Medical Therapy
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  • Medicine, Biology
    Journal of the American Geriatrics Society
  • 1991
Epidemiologic studies in castrates strongly support the key role of the testis in the pathogenesis of benign prostatic hyperplasia (BPH). Since the testis secretes androgen and estrogen, both of
Finasteride, an inhibitor of 5 alpha-reductase, suppresses prostatic dihydrotestosterone in men with benign prostatic hyperplasia.
It is concluded that finasteride causes profound decrease in prostatic dihydrotestosterone levels in the prostates of men with benign prostatic hyperplasia.
The effect of finasteride in men with benign prostatic hyperplasia.
  • P. Walsh
  • Medicine
    The Journal of urology
  • 1993
The treatment of benign prostatic hyperplasia with 5 mg of finasteride per day results in a significant decrease in symptoms of obstruction, an increase in urinary flow, and a decrease in prostatic volume, but at a slightly increased risk of sexual dysfunction.
Relative potency of testosterone and dihydrotestosterone in preventing atrophy and apoptosis in the prostate of the castrated rat.
Whereas DHT is more potent than testosterone at stimulating prostate epithelial cell function as measured by ductal mass, the two androgens are equipotent at preventing prostate cell death after castration, which explains why finasteride causes prostate involution in the rat with minimal evidence of prostate cellDeath.
Deletion of steroid 5α-reductase 2 gene in male pseudohermaphroditism
The results verify the existence of at least two 5α-reductases in man and provide insight into a fundamental hormone-mediated event in male sexual differentiation.
Testosterone at high concentrations interacts with the human androgen receptor similarly to dihydrotestosterone.
The results suggest that the weaker androgenic potency of testosterone compared to that of dihydrotestosterone resides in its weaker interaction with the androgen receptor, most clearly demonstrable as an increase in the dissociation rate of testosterone from the receptor.
Expression and regulation of steroid 5 alpha-reductase 2 in prostate disease.
Investigation of the expression of the type 2 isozyme of 5 alpha-reductase in benign prostatic hyperplasia and prostate cancer shows that androgen ablation therapies substantially decrease isozyme expression in the epididymis but have a lesser effect in the prostate.
Deletion of steroid 5 alpha-reductase 2 gene in male pseudohermaphroditism.
The results verify the existence of at least two 5 alpha-reductases in man and provide insight into a fundamental hormone-mediated event in male sexual differentiation.